Study Notes: Corticosteroids (Anti-inflammatory Steroids)
I. Introduction
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Corticosteroids = anti-inflammatory steroids.
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Two parts of the name:
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Steroid → hormone.
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Cortico → related to cortisol (natural stress hormone).
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Distinction: Not anabolic (muscle growth) steroids → these primarily reduce inflammation.
II. Cortisol & Corticosteroid Basics
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Cortisol is made via:
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Hypothalamus → ACTH → adrenal glands → cortisol release.
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Negative feedback loop: High cortisol inhibits hypothalamus.
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Receptors:
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Glucocorticoid receptor (main therapeutic target).
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Mineralocorticoid receptor (electrolyte balance).
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III. Glucocorticoid Effects (3 main pathways)
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Anti-inflammatory
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Inhibits mediators: phospholipase A₂, IL-6, TNF-α, etc.
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↓ Inflammation (skin, lungs, hives, etc.).
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Immunosuppression
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Inhibits T-cells & B-cells → ↓ immune response.
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Useful in transplant patients & autoimmune diseases.
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Metabolic (liver)
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↑ Glucose release (glycogen → glucose).
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Stress response = more energy.
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Watch for hyperglycemia in diabetics.
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IV. Mineralocorticoid Effects
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Sodium & water retention.
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Potassium excretion.
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Maintains fluid/electrolyte balance.
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Clinical use: Addison’s disease, adrenal insufficiency.
V. Dosage Forms
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Topical: Creams/ointments (hydrocortisone).
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Oral: Prednisone, methylprednisolone (dose packs).
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Inhaled/Intranasal: Symbicort, Flonase (asthma, allergies).
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IV/Injectable: Dexamethasone (hospital setting).
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Naming clue: Ends in -isone or -asone.
VI. Clinical Uses
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Inflammation (skin irritation, tissue damage).
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Allergic reactions (hives, anaphylaxis).
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Asthma/COPD (inhaled steroids).
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Autoimmune diseases (Crohn’s, MS, lupus).
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Cancer therapy (part of regimens, premeds).
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Adrenal insufficiency (mineralocorticoid use).
VII. Dosing & Potency
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Hydrocortisone = baseline potency (1×).
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Prednisone ≈ 4× stronger.
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Methylprednisolone ≈ stronger still.
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Dexamethasone = 25–30× stronger.
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Relative potency + mineralocorticoid activity guide drug choice.
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Taper required if therapy > ~6–7 days to prevent adrenal crisis.
VIII. Side Effects
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Weight gain (reversible).
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Fat redistribution (Cushing’s syndrome, “moon face”).
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Edema (fluid buildup).
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Osteoporosis (long-term use).
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Altered mental status (mood/behavior changes).
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Hyperglycemia (liver glucose release).
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Hypertension.
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Peptic ulcers.
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Increased infection risk (immune suppression).
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Adrenal crisis (abrupt stop → life-threatening).
IX. Quiz
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Well-known adverse effect of chronic systemic glucocorticoid use?
→ Osteoporosis. -
Common sign of iatrogenic Cushing’s syndrome?
→ Moon face (fat redistribution). -
Why taper after prolonged therapy?
→ Prevent adrenal crisis (due to HPA-axis suppression). -
Bone-related preventive measure in long-term therapy?
→ Calcium + Vitamin D supplementation, consider bisphosphonates.
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